ArticleJournal of neuroinflammation2024
Exercise training upregulates CD55 to suppress complement-mediated synaptic phagocytosis in Parkinson's disease.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Physical exercise and inflammation in Parkinson's disease: a review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Pooled it
- Multiomics Integration of Parkinson's Disease Datasets Reveals Unexpected Roles of IRE1 in Its Pathology.International journal of molecular sciences · 2025Pooled it
- Study of blood linear RNA nominates CD55 and DLD as early-stage biomarkers for Parkinson's disease.Brain : a journal of neurology · 2026Article
- Sex-aware causal inference assessment of the immune system in complex neurodegenerative diseases.Brain : a journal of neurology · 2026Article
- Complement dysregulation during the early phases of synucleinopathy.Acta neuropathologica · 2026Article
- Microglia-mediated synaptic pruning in neural circuit remodeling: multidimensional control in homeostasis and neuropathology.BMC medicine · 2026Review
- The complement C3-microglial axis in depression of Parkinson's disease: from mechanism to therapeutic intervention.EBioMedicine · 2026Article
- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
- Exercise training promotes nerve cell repair and regeneration after spinal cord injury.Neural regeneration research · 2026Article
- Sex-specific effects of exercise on motor coordination and extended basal ganglia physiology.bioRxiv : the preprint server for biology · 2026Article
- Bindarit attenuates brain injury and neuroinflammation in status epilepticus by disrupting C3/C3aR signaling and modulating microglia-astrocyte interactions.Cell communication and signaling : CCS · 2026Article
- Indirubin and Retinoic Acid Show Binding Affinity to Monocyte Biomarker CSF3R in Parkinson's Disease.Journal of clinical laboratory analysis · 2026Article
- Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Cuproptosis-associated genesFrontiers in immunology · 2026Article
- New perspectives on molecular mechanisms underlying exercise-induced benefits in Parkinson's disease.NPJ Parkinson's disease · 2025Review
- Exercise modulation of BDNF/TrkB signaling in Parkinson's disease: an evidence-calibrated review of neuroprotective mechanisms, biomarker limitations, and translational gaps.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The primary pathological change in Parkinson's disease (PD) is the progressive degeneration of dopaminergic neurons in the substantia nigra. Additionally, excessive microglial activation and synaptic loss are also typical features observed in PD samples. Exercise trainings have been proven to improve PD symptoms, delay the disease progression as well as affect excessive microglial synaptic phagocytosis. In this study, we established a mouse model of PD by injecting mouse-derived α-synuclein preformed fibrils (M-α-syn PFFs) into the substantia nigra, and demonstrated that treadmill exercise inhibits microglial activation and synaptic phagocytosis in striatum. Using RNA-Seq and proteomics, we also found that PD involves excessive activation of the complement pathway which is closely related to over-activation of microglia and abnormal synaptic function. More importantly, exercise training can inhibit complement levels and complement-mediated microglial phagocytosis of synapses. It is probably triggered by CD55, as we observed that CD55 in the striatum significantly increased after exercise training and up-regulation of that molecule rescued motor deficits of PD mice, accompanied with reduced microglial synaptic phagocytosis in the striatum. This research elucidated the interplay among microglia, complement, and synapses, and analyzed the effects of exercise training on these factors. Our work also suggested CD55 as a complement-relevant candidate molecule for developing therapeutic strategies of PD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.